This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The goal of this research is to begin to test the hypothesis that an abnormally robust systemic, rather than pulmonary, cytokine and intercellular adhesion molecule-1 (ICAM-I, known also as CD54) response to exercise in asthmatic children may play a role in the phenomenon of exercise induced bronchoconstriction (EIB). This new hypothesis is based on observations recently made in the laboratory of Dr. Dan Cooper. It is now clear that relatively brief episodes of intense exercise stimulate proinflammatory cytokines (namely, interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) and ICAM-I expression on peripheral blood mononuclear cells in healthy children with no history of asthma. This is an intriguing finding since proinflammatory mediators like IL-1 and ICAM-I may play a role in bronchial asthma, and exercise-induced wheezing is found in the vast majority of patients with childhood asthma. Thus, it is reasonable to hypothesize that these systemic inflammatory responses to exercise may be abnormally robust in asthmatic children and contribute to the mechanisms responsible for EIB. This hypothesis has not yet been addressed in either adults or children.